Abstract
BackgroundPapillary thyroid carcinoma (PTC) is the most common malignant thyroid neoplasm comprising 80–90% of all thyroid malignancies. Molecular changes in thyroid follicular cells are likely associated with the development of PTC. Mutations in serine/threonine-protein kinase (BRAF) and Rat sarcoma viral oncogene homolog (RAS) are commonly seen in PTC.MethodsIn total, 90 cases of PTC are randomly selected from archive paraffin blocks and 10μm sections were cut and processed for DNA extraction. BRAF V600E mutation and 8 types of KRAS mutations were investigated using Real Time PCR.ResultsBRAF V600E mutation was identified in 46% of PTC while KRAS mutations were seen in 11% of PTC. There was significant correlation between BRAF V600E mutation and PTC larger than 5cm in diameter, positive surgical margin and lymph node metastasis. BRAF V600E mutation was significantly higher in patients with less than 55-year of age than those more than 55-year of age. BRAF V600E mutation was significantly higher in patients with family history of thyroid cancer than those without. There was no significant difference in BRAFV600E mutation between males and females, PTC classic and follicular variants, unifocal and multifocal PTC. There was a significant higher percentage of BRAF V600E mutation in classic PTC than papillary microcarcinoma variant. There was no significant age, gender, histologic type, tumor size, lymph node metastasis, tumor focality, and surgical margin status differences between KRAS mutated and non-mutated PTC.ConclusionBRAF V600E and KRAS mutation are seen in a significant number of PTC in the UAE. BRAF mutation is significantly correlated with large tumor size, positive surgical margins and lymph node metastasis suggesting an association between BRAF V600E mutation and tumor growth and spread.
Highlights
Thyroid cancer is the most common endocrine malignancy and clinical thyroid cancer accounts for 1–2% of all cancers [1]
BRAF V600E mutation was identified in 46% of Papillary thyroid carcinoma (PTC) while KRAS mutations were seen in 11% of PTC
BRAF V600E mutation was significantly higher in patients with family history of thyroid cancer than those without
Summary
Thyroid cancer is the most common endocrine malignancy and clinical thyroid cancer accounts for 1–2% of all cancers [1]. Molecular alterations in the sequence composition of cellular molecules such as DNA, RNA, and proteins usually precede the development of PTC. These alterations are frequently initiated by specific mutations in growth signal genes such as serine/threonine-protein kinase (BRAF) or Rat sarcoma viral oncogene homolog (KRAS) which will be translated into oncoproteins that lead to uncontrolled growth signals within affected follicular cells [5,6,7]. BRAF and KRAS mutations are commonly seen in PTC [5]. Molecular changes in thyroid follicular cells are likely associated with the development of PTC. Mutations in serine/threonine-protein kinase (BRAF) and Rat sarcoma viral oncogene homolog (RAS) are commonly seen in PTC
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